Somatostatin as modulator of vagal effects on cardiac rhythm

Pokrovskii, V. M.; Osadchii, Oleg E.; Курзанов, А. Н.

doi:10.1007/bf00790043

Cited by 4 publications

(5 citation statements)

References 8 publications

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“…The interventions (including the pharmacological ones) that increase the initial HR promote the inhibiting effect of the vagus, while a decrease in HR leads to an opposite effect. Previously, we observed a decrease in VCE after administration of taurine or pilocarpine (compounds that decelerate HR) [3,4] and an increase in this effect after administration of epinephrine, serotonin, or neurotensin (compounds that accelerate HR) [2,3]. Thus, suppression of VCE and its tonic component caused by SS is probably associated with deceleration of initial HR.…”

Section: Resultsmentioning

confidence: 86%

Cardiotropic effects of somatostatin and its antagonists

et al. 1997

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Somatostatin reduces cardiac rhythm in cats, the effect being abolished by the Mcholinolytic methacin, the ganglioblocker benzohexonium, or somatostatin antagonist, Somatostatin suppresses vagal chronotropic effect by reducing its tonic component, while the synchronizing vagal component increases. The antagonist of somatostatin exerts an opposite effect: it eliminates the influence of somatostatin on the tonic vagal component and reverses its effect on the synchronizing component. Key Words: somatostatin; somatostatin antagonist; vagus; cardiac rhythmThere is considerable evidence indicating that somatostatin (SS) modulates cardiac activity. Somatostatin slows down the heart beat [10,15], elicits a negative inotropic effect [7], and decreases myocardial conductivity [6,15]. It was interesting to compare cardiotropic effects of SS with the effects of SS peptide antagonist. In the present study we examined the effects of these compounds on heart rate (HR) and parasympathetic regulation of heart rhythm in cats. MATERIALS AND METHODSExperiments were performed on 42 cats weighing 2.5-3.5 kg. The animals were anesthetized with chlomlose (75 mg/kg) and Nembutal (15 mg/qqg) and transferred to artificial ventilation. Both preparations were injected intraperitoneally. The peripheral end of the right vagus was stimulated by bursts of 3, 6, or 9 rectangular pulses (2 msec, 40 Hz) with an amplitude of 5-6 thresholds. A unipolar probe was inserted into the fight atrium via femoral vein for enhanced ECG recording. The P wave indicated the beginning of the intervalogram for SS (Sigma). The SS antagonist (7-amino-heptanoyl-Phe-D-Trp-Lys-Thr[Bzl]) was infused intravenously in 0.5 ml normal saline. The RESULTSIn the first series of experiments (n=7) we studied the effect of SS (1.3• =8 M) on HR. This peptide reduced HR from 195.6+5.2 to 180.5+4.4 beats/rain, i.e., by 7.7% (p<0.05), the latency of the effect being 23.6+3.5 sec. The maximum length of cardiac cycle was observed 45.7+4.6 sec after the onset of chronotropic reaction. Bradycardia was preserved for 6-15 rain after administration of the peptide. Repeated administrations of SS induced no tachyphylaxis. The effect of SS was abolished by pretreatment with the M-cholinolytic methacin (0.0025 mg/kg), the ganglioblocker benzohexonium (8 mg/kg), or SS antagonist (2.6x10 -8 M). The SS antagonist (n=10) had no effect on HR.In the second series of experiments we investigated the influence of SS on the dynamics of vagat chronotropic effect (VCE) induced by pulse stimulation of the vagus. In established vagal bradycardia cardiac contractions were synchronous with the rhythm of vagal stimulation. For example, with an initial HR of 194.3+4.5 beats/rain a 6-pulse stimulation of the vagus led to synchronization of vagal and cardiac rhythms which lasted from 103.5+3.4 to 84.6+4.3

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Section: Resultsmentioning

confidence: 86%

Cardiotropic effects of somatostatin and its antagonists

et al. 1997

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“…Modulating effects of the peptides are usually considered on the basis of their presynaptic effect manifested in the change of the amount of transmitter released from the nerve terminals. However, this approach is probably of little practical use in analysis of the peptide effect on the dynamics of the vagal synchronizing component, because its value only slightly depends on changes in the efficient concentration of acetylcholine [6]. The effect of some peptides at the postsynaptic level is similar to the effects observed during stimulation of VN.…”

Section: Resultsmentioning

confidence: 94%

“…The nature of this phenomenon cannot be explained entirely by the classical cholinergic mechanisms: the regulator peptides play a certain role in it [6,15]. Specifically, it is shown that both somatostatin (SS) and Met-enkephalin (ME) increase the frequency range in which vagal stimulation controls cardiac rhythm [7,15].…”

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confidence: 99%

Specificity of vagotropic peptide action under subtotal blockade of cardiac M-cholinoreceptors

Osadchii

Pokrovskii

1998

Bull Exp Biol Med

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In experiments on anesthetized cats modulation of the components of vagal chronotropic effects by somatostatin and Met-enkephalin is studied under complete block of Mcholinoreceptors caused by administration of the M2-cholinoblocker Imperialine or the subthreshold doses of the non-selective M-cholinolytic agent methacine. A differential character of vagotropic effect of peptides is revealed, which is manifested in restoration of the synchronizing vagal component that was decreased by cholinolytics, while a similar effect on the inhibitory tonic vagal influence was absent.

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“…Thus, the nonselective M-receptor blocker methacine decreases the synchronizing but not tonic component [4]. On the other hand, the cholinergic agonist pilocarpine reduces the tonic inhibitory effect of the VN stimulation leaving the synchronizing component unaffected [2]. These data suggest that diflerent VCE components are mediated by different subtypes of muscarinic receptors, which are distinguished by their affinity to the corresponding ligands.…”

Section: R Es U Ltsmentioning

confidence: 98%

Dynamics of vagal chronotropic effects during blockade of different types of muscarinic cholinergic receptors

Osadchii

Pokrovskii

1999

Bull Exp Biol Med

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Different changes in vagal chronotropic effects were observed in cats under blockade of various types of muscarinic cholinergic receptors. Burst stimulation of the vagus nerve caused synchronization of the vagal and cardiac rhythms, which was potentiated by M a and M 3 receptor antagonists and suppressed by the M 2 blocker gallamine. The components of the vagal chronotropic effect showed different sensitivity to selective M-cholinolytics.Key Words: muscarini cholinergic receptors; vagal chronotropic effect Heterogenous population of muscarinic cholinergic receptors includes at least 5 subtypes which are distinguished by their structure, location, and functional properties [7]. In the myocardium, M2receptors are the predominant type of receptors. They mediate the inhibitory effects of the vagus nerve (VN) stimulation. However, there is evidence that other types of cholinergic receptors are also implicated in the regulation of cardiac activity. For instance in rats and guinea pigs, the intracardial neurons contain RNAs encoding four types of muscarinic receptors (M1-M 4) [9]. Receptors of different types may play different functional roles. For instance, in dogs MI receptor blockade significantly weakened the vagal chronotropic effect (VCE), but did not affect the vagal influence on the myocardial conductivity and contractility [5,12].These findings can be used in the analysis of VCE mechanisms. Along with the inhibitory tonic component, the chronotropic effect contains a synchronizing component that controls cardiac rhythm under conditions of VN stimulation [13]. These components are probably associated with different muscarinic receptors. In this study we checked up this hypothesis. MATERIALS AND METHODSExperiments were carried out on 27 cats weighing 3-4 kg anesthetized with intraperitoneal Chloralose-NemDepartment Physiolo9y, Kuban Medical Academy, Krasnodar butai mixture (75:15 mg/kg) and 'artificially ventilated. The peripheral end of the right VN was stimulated with short 40 Hz trains of 3, 6, or 9 rectangular pulses of 0.2 msec duration and 5-6 thresholds' intensity. Amplified ECG was recorded by a unipolar probe inserted through the femoral vein into the right atrium. The following selective M-receptor antagonists were used: pirenzepine (M1), gallamine (M2), and 4-diphenylacetoxy-N-(2-chlorethyl)-piperidine (4-DAMP. M3) [6]. The drugs (0.002-0. 2 mg/kg ) were infused intravenously. The data were analyzed statistically by the method of direct differences [ 1 ].

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Somatostatin as modulator of vagal effects on cardiac rhythm

Cited by 4 publications

References 8 publications

Cardiotropic effects of somatostatin and its antagonists

Cardiotropic effects of somatostatin and its antagonists

Specificity of vagotropic peptide action under subtotal blockade of cardiac M-cholinoreceptors

Dynamics of vagal chronotropic effects during blockade of different types of muscarinic cholinergic receptors

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